engleski

Kinetics of tissue iron in experimental autoimmune encephalomyelitis in rats

Iron is an essential trophic factor that plays a key role in vital cell functions. It is indispensable cofactor for enzymes involved in cell proliferation, respiration, folate metabolism and DNA synthesis, having a crucial role in metabolic pathways involved in electron transfer and ATP production. The redox potential of Fe2+/Fe3+ favors its use in a number of protein complexes, but as a part of the Fenton reaction ferrous iron may also catalyze the conversion of hydrogen peroxide to highly reactive hydroxyl radicals that damage DNA, proteins and lipids. Therefore, the maintenance of iron homeostasis in the body and in the cells must be balanced, to ensure enough iron for the metabolism, but to avoid excessive, toxic levels of iron that provoke oxidative tissue injuries. To elucidate the role of iron in the pathomechanisms of autoimmune CNS disorders we estimated the tissue concentrations of Fe2+ in the brain, spinal cord (SC) and liver in monophasic and chronic relapsing (CR) forms of experimental autoimmune encephalomyelitis (EAE), induced in Dark Agouti (DA) strain of rats, by subcutaneous injection of myelin basic protein (MBP) in complete Freund’s adjuvant (CFA) or by bovine brain homogenate (BBH) in CFA, respectively. Control rats were treated with CFA or with saline solution. The data obtained by clinical assessment and by inductively coupled plasma spectrometry have shown that in both monophasic EAE (induced by MBP+CFA) and in CR-EAE (induced by BBH+CFA) the attacks of disease were followed by high accumulation of iron in the liver (on the 12th post-immunization day, and on the 12th and the 22nd day). Simultaneously, in monophasic EAE decreased the concentration of Fe2+ in the brain (during the remission phase) and in the cervical spinal cord (during attacks and remission). Similarly, in CR-EAE the lower iron content was found in cervical spinal cord during the second attack of disease. The data point to regulatory effects of iron and hepatic trace elements regulating mechanisms in the pathogenesis of EAE.

chronic relapsing encephalomyelitis; iron; brain; spinal cord; liver

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